摘要：

The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca 2+ from the incubation medium abolished [ 3 H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC 50 values for agonists were unaltered in the absence of Ca 2+ . Removal of Ca 2+ by preincubation with EGTA (0.5 m M ) abolished all responses, but complete restoration was achieved by replacement of Ca 2+ . The EC 50 for Ca 2+ for histamine-stimulated [ 3 H]inositol phosphate accumulation was 80 M . Noradrenaline-stimulated breakdown was antagonised by manganese (IC 50 1.7 m M ), but not by the calcium channel blockers nitrendipine or nimodipine (30 M ). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC 50 of 2 M , and this response was blocked by EGTA. Omission of Ca 2+ or preincubation with EGTA or Mn 2+ (EC 50 = 230 M ) greatly enhanced the incorporation of [ 3 H]inositol into phospholipids. The IC 50 for Ca 2+ in inhibiting incorporation was 25 M . The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca 2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate.

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